4.5 Review

Trimethylamine N-Oxide Generated by the Gut Microbiota: Potential Atherosclerosis Treatment Strategies

Journal

CURRENT PHARMACEUTICAL DESIGN
Volume 28, Issue 35, Pages 2914-2919

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612828666220919085019

Keywords

CVD; atherosclerosis; TMAO; gut microbiota; treatment; FMO3; diet; renal function

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Cardiovascular diseases, particularly atherosclerotic cardiovascular diseases, are a major global burden. Emerging research on gut microbiota has revealed the significant role of trimethylamine oxide (TMAO), a metabolite from gut microbes, in atherosclerosis. Targeting TMAO may offer potential therapeutic strategies for atherosclerosis.
Cardiovascular diseases (CVD) have become a disease burden that plagues the world, and a large proportion of the world's mortality currently stems from atherosclerotic CVD. In addition to traditional therapies, we need to find more therapeutic targets and strategies in scientific research to address this challenge. In recent years, as research on gut microbiota has continued, there has been a clearer understanding of the role that metabolites from gut microbes play during atherosclerosis (AS). A growing body of research suggests that trimethylamine oxide (TMAO) is an independent risk factor for CVD and that gut microbe-dependent TMAO plays a critical role in AS. Therefore, interventions targeting TMAO have the potential to become a new therapeutic strategy for AS. This review provides a brief overview of the relationship between TMAO and atherosclerosis. More importantly, several potential atherosclerosis treatment strategies targeting TMAO and its metabolic pathways have been revealed by recent studies and will be the focus of this review. This review summarizes possible therapeutic strategies in terms of change of diet, adjustment of gut microbiota, suppression of liver enzyme activity, and improvement of renal function, in the hope of providing new insights for developing efficient and cost-effective treatment and prevention for AS.

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